Publication: Atherosclerosis and oxidative stress
Authors
Bonomini, F. ; Tengattini, S. ; Fabiano, A. ; Bianchi, R. ; Rezzani, R.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
This review focuses on the morphological
features of atherosclerosis and the involvement of
oxidative stress in the initiation and progression of this
disease. There is now consensus that atherosclerosis
represents a state of heightened oxidative stress
characterized by lipid and protein in the vascular wall.
Reactive oxygen species (ROS) are key mediators of
signaling pathways that underlie vascular inflammation
in atherogenesis, starting from the initiation of fatty
streak development, through lesion progression, to
ultimate plaque rupture. Plaque rupture and thrombosis
result in the acute clinical complications of myocardial
infarction and stroke. Many data support the notion that
ROS released from nicotinamide adenine dinucleotide
phosphate (NADPH) oxidase, myeloperoxidase (MPO),
xanthine oxidase (XO), lipoxygenase (LO), nitric oxide
synthase (NOS) and enhanced ROS production from
dysfunctional mitochondrial respiratory chain, indeed,
have a causatory role in atherosclerosis and other
vascular diseases. Moreover, oxidative modifications in
the arterial wall can contribute to the arteriosclerosis
when the balance between oxidants and antioxidants
shifts in favour of the former. Therefore, it is important
to consider sources of oxidants in the context of
available antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx),
glutathione reductase and transferases thiol-disulfide
oxidoreductases and peroxiredoxins. Here, we review
also the mechanisms in which they are involved in order
to accelerate the pace of the discovery and facilitate
development of novel therapeutic approaches.
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